Although studies have demonstrated the efficacy of the new anti-epileptic on the block, Pregabalin, in the treatment of Generalized Anxiety Disorder and Social Anxiety Disorder, there is no study so far of such efficacy for the treatment of depression. This case study in a patient with chronic major depression demonstrates that Pregabalin could be an effective augmenting agent to other anti-depressants, e.g. SSRI's and SNRI's. This added property of Pregabalin may be related to its probable GABA-ergic mechanism of action that could be soon the emerging treatment pathway for achieving better remission in chronic depression that is yet clinically problematic.
The old classification of depression as reactive and endogenous, which are still observed in clinical practice, both cannot be accommodated under the current rubric of major depression. This is because psychiatric nosology under the Diagnostic and Statistical Manual of Mental Disorders (DSM) and its latest fifth edition (DSM-V) is still descriptive and not etiologic. The aim of this review was to revisit reactive and endogenous categories of depression from the perspective of today's understanding of etiological pathways. From an epigenetic perspective, the old dichotomy of reactive versus endogenous is interrelated through the impact of the environment (e.g., stress). This includes familial or prenatal depression, where the environmental impact is before birth, or childhood depression, where the early life stress is the precipitating factor to genetic susceptibility. In conclusion, searching for both environmental impact (e.g., stressors) and genetic predispositions in depression, even at a clinical level, could help clinicians with better therapeutic decisions.
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